Human immunodeficiency virus (HIV) is a retrovirus that causes acquired immunodeficiency syndrome (AIDS). HIV-1 is the most common and pathogenic strain of the virus. Although HIV-1 infection can be suppressed with any one of several different combination anti-retroviral therapies (ART), such a therapy must be maintained for the life of a patient because it does not eliminate a reservoir of latently infected cells even after years of ART (Siliciano, et al., Nat Med, 2003. 9(6): pp. 727-8.). As a result, ART termination follows by rapid viral rebound (Davey, et al., Proc. Natl. Acad. Sci. U.S.A. 1999. pp. 15109-15114). To date, all attempts to alter the reservoir by intensifying ART, by including additional anti-retroviral drugs (Dinoso, et al., Proc Natl Acad Sci U.S.A., 2009. 106(23) pp. 9403-8 and Gandhi, et al., PLoS Med, 2010. 7(8)), or by administration of global T-cell activators or inducers of viral transcription, in the presence of ART, have failed (Archin, et al., J. Infect. Dis. 2014. pp. 1-26; Dybul, et al., Infect Dis, 2002. 185(1): pp. 61-8; Lafeuillade, et al., J Acquir Immune Defic Syndr, 2001. 26(1): p. 44-55; and Prins, et al., AIDS, 1999. 13(17): p. 2405-10). Thus, there is a need for methods and agents for prevention or disruption of the establishment or maintenance of HIV-1 latent reservoirs.